Hypersensitivity

Question 1

What is an antigen?

Answer 1

Any molecule that can be recognised by an antibody or the adaptive immune system.

Question 2

What does IgE do in relation to mast cells?

Answer 2

Primes mast cell.

Question 3

What is the only class of antibody that can cross the placenta?

Answer 3

IgG

Question 4

What class of antibody can cross muscosal epithelium?

Answer 4

IgA and sometimes IgM.

Question 5

What immunoglobulin activates classical complement pathway?

Answer 5

IgM and IgG3.

Question 6

What class of antibody binds to Fc receptors on phagocytes?

Answer 6

IgG

Question 7

What class of antibody is present on membrane of mature B cells?

Answer 7

IgM.

Question 8

What is type I hypersensitivity mediated by?

Answer 8

IgE.

Question 9

Which T helper cells activate B cell in type 1 hypersensitivity?

Answer 9

Th2 and T follicular helper cells.

Question 10

What cytokines cause B cells to produce IgE (class switch) in type 1 hypersensitivity?

Answer 10

IL-4 and IL-13.

Question 11

Which innate immune system cells have a high affinity for IgE?

Answer 11

Mast cells and basophils.

Question 12

What cells are seen in early phase of type 1 hypersensitivity?

Answer 12

Mast cells.

Question 13

What is seen later (within few hours) on in type 1 hypersensitivitiy?

Answer 13

Recruitment of neutrophils.

Question 14

What do we seen in late response (3-5 days) to type 1 hypersensitivity?

Answer 14

High frequencies of eosinophils.

Question 15

What does type II hypersensitivity involve?

Answer 15

Destruction of cells by IgG or IgM antibody bound to antigens present on the surface of the cells.

Question 16

How can antibodies cause type 2 hypersensitivity?

Answer 16

Activation of complement system (C3a, C4a and C5a) recruit neutrophils which can destroy cells by degranulation. Formation of MAC complex (C5b, C6-C9) which can creates a channel in cell membrane leading to lysis. Opsonisation and phagocytosis. Antibody dependent cell mediated cytotoxicity where NK cells bind to fc region and release toxic granules. Antibody mediated cellular dysfunction where antibody binds to receptor blocking it or activating it.

Question 17

What is type 3 hypersensitivity?

Answer 17

Immune complex driven disease. Immune complexes cannot be efficiently cleared, immune complexes end up being deposited in the blood vessel walls and tissues, promoting inflammation and tissue damage.

Question 18

How can type 3 hypersensitivity lead to tissue damage?

Answer 18

Activation of complement system (C3a,C4a,C5a) increase vascular permeability which can lead to oedema. Neutrophils can’t phagocytose complexes and so degranulate which can lead to vasculitis.

Question 19

What is an immune complex?

Answer 19

Non-cell bound antigen-antibody complexes which are normally cleared through the activity of the immune system.

Question 20

What class of disease involve type 3 hypersensitivity?

Answer 20

Auto immune disease.

Question 21

What is type IV hypersensitivity?

Answer 21

Delayed type hypersensitivity involving T cells.

Question 22

How quick is type I hypersensitivity?

Answer 22

Immediate.

Question 23

What is the first exposure to an allergen called in type 1 hypersensitivity?

Answer 23

Sensitization.

Question 24

What causes mast cell to degranulate in hypersensitivity 1?

Answer 24

Cross linkage of IgE primed mast cell.

Question 25

Why does anaphylaxis happen in type 1 hypersensitivity?

Answer 25

Release of histamines from mast cells cause blood pressure drop.

Question 26

Difference between type II hypersensitivity and type III?

Answer 26

Type II involves antibodies binding to antigens on cell surfaces while type III involves antibodies binding to soluble molecules to form complexes. Type 2 inflammation occurs where antigen is present in the body while type 3 is where the antigen-antibody complexes are deposited. Type 2 small amount of complement is produced while type 3 lots of complement proteins are released. Levels of complement protein can be tracked to see progression of type 3 hypersensitivity.

Question 27

Why is type IV delayed?

Answer 27

Memory T cell response is slightly slow. 48 -72 hours.

Question 28

What causes contraction of pulmonary smooth muscle?

Answer 28

Leukotrienes and prostaglandins.

Question 29

What are the rate limiting molecules in all hypersensitivity reaction?

Answer 29

Antigens.

Question 30

What are the characteristics of the infiltrate in a delayed hypersensitivity reaction?

Answer 30

An infiltrate composed of helper T cells and macrophages.

Question 31

What is a hapten? Give an example

Answer 31

A small molecule which on its own is not antigenic, but when associated with a large carrier such as a protein can form an antigen. Penicillin binding to surface antigen on red blood cells causing haemolysis.

Question 32

When is a coombs test done?

Answer 32

Autoimmune hemolytic anemia. Drug-induced immune hemolytic anemia.

Question 33

Describe and explain the coombs test

Answer 33

Blood sample from patient is taken. Red cells from patient are washed to remove any unbound antibodies. Coombs reagent (anti human globulin) is added. If antibody is present on the surface of the red blood cells this results in agglutination.